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Clinical EEG and Neuroscience Apr 2008We have examined language processing using ambiguous words (homographs like panel or toast) and rapid or slow presentation rates while recording event-related brain... (Review)
Review
We have examined language processing using ambiguous words (homographs like panel or toast) and rapid or slow presentation rates while recording event-related brain potentials (ERPs). Homographs allow for tracking the train of thought at points of lexical ambiguity and detecting modulation of associative threads by previous context. Rapid presentation rates stress automatic semantic activation, and slow rates stress controlled verbal working memory contextual modulation. In conjunction with reaction times and performance, ERPs allow for objective measurement of activity related to language processing from word presentation through overt behavioral response. Smaller N400 to related and unrelated items at short stimulus onset asynchronies (SOAs), the presence of a semantic bias, and large N400 to related and unrelated items at long SOAs are present in schizophrenia. We describe a model of initial semantic memory hyper-priming and subsequent decay of information in verbal working memory stores, the activation-maintenance model of schizophrenic thought disorder hypothesized to underlie the thought disorder in schizophrenia.
Topics: Cognition Disorders; Electroencephalography; Evoked Potentials; Humans; Memory Disorders; Reading; Schizophrenia; Semantics
PubMed: 18450179
DOI: 10.1177/155005940803900217 -
Neuropharmacology Jan 2012In addition to its role in development and cell proliferation, β-catenin has been implicated in neuronal synapse regulation and remodeling. Here we review basic... (Review)
Review
In addition to its role in development and cell proliferation, β-catenin has been implicated in neuronal synapse regulation and remodeling. Here we review basic molecular and structural mechanisms of synaptic plasticity, followed by a description of the structure and function of β-catenin. We then describe a role for β-catenin in the cellular processes underlying synaptic plasticity. We also review recent data demonstrating that β-catenin mRNA and protein phosphorylation are dynamically regulated during fear memory consolidation in adult animals. Such alterations are correlated with a change in the association of β-catenin with cadherin, and deletion of the β-catenin gene prevents fear learning. Overall, the extant data suggest that β-catenin may function in mediating the structural changes associated with memory formation. This suggests a general role for β-catenin in synaptic remodeling and stabilization underlying long-term memory in adults, and possible roles for dysfunction in the β-catenin pathway in disorders of memory impairment (e.g. Alzheimer's Disease) and in disturbances in which emotional memories are too strong or resistant to inhibition (e.g. fear learning in Posttraumatic Stress Disorder). Further understanding of the β-catenin pathway may lead to better appreciation for the structural mechanisms underlying learning and memory as well as provide novel therapeutic approaches in memory related disorders. This article is part of a Special Issue entitled 'Anxiety and Depression'.
Topics: Animals; Anxiety; Cell Adhesion Molecules; Depression; Humans; Memory Disorders; Models, Neurological; Neuronal Plasticity; Nonlinear Dynamics; Synapses; beta Catenin
PubMed: 21903109
DOI: 10.1016/j.neuropharm.2011.08.032 -
Frontiers in Bioscience (Scholar... Jan 2011Schizophrenia is a remarkably complex disorder with a multitude of behavioral and biological perturbations. Cognitive deficits are a core feature of this disorder, and... (Review)
Review
Schizophrenia is a remarkably complex disorder with a multitude of behavioral and biological perturbations. Cognitive deficits are a core feature of this disorder, and involve abnormalities across multiple domains, including memory, attention, and perception. The complexity of this debilitating illness has led to a view that the key to unraveling its pathophysiology lies in deconstructing the clinically-defined syndrome into pathophysiologically distinct intermediate phenotypes. Accumulating evidence suggests that one of these intermediate phenotypes may involve phospholipid signaling abnormalities, particularly in relation to arachidonic acid (AA). Our data show relationships between levels of AA and performance on tests of cognition for schizophrenia patients, with defects in AA signaling associated with deficits in cognition. Moreover, dopamine may moderate these relationships between AA and cognition. Taken together, cognitive deficits, dopaminergic neurotransmission, and bioactive lipids have emerged as related features of schizophrenia. Existing treatment options for cognitive deficits in schizophrenia do not specifically target lipid-derived signaling pathways; understanding these processes could inform efforts to identify novel targets for treatment innovation.
Topics: Animals; Cognition; Dopamine; Eicosanoids; Fatty Acids, Unsaturated; Humans; Memory Disorders; Models, Neurological; Phospholipids; Schizophrenia; Signal Transduction; Synaptic Transmission
PubMed: 21196378
DOI: 10.2741/s153 -
Journal of Affective Disorders Jul 2016Previous studies investigated the impact of brain-derived neurotrophic factor (BDNF) val66met (rs6265) on hippocampus volumes and neurocognition in bipolar disorders...
BACKGROUND
Previous studies investigated the impact of brain-derived neurotrophic factor (BDNF) val66met (rs6265) on hippocampus volumes and neurocognition in bipolar disorders (BD), but the results were not consistent. This study aimed to investigate the effect of BDNF polymorphism on hippocampus volumes and memory performance in well-characterized adult populations diagnosed with type I BD (BD-I) and major depressive disorder (MDD) compared with healthy controls (HC).
METHODS
48 BD-I patients, 33 MDD patients and 60 HC were genotyped for BDNF rs6265 using DNA isolated from white blood cells. Individuals with val/met and met/met genotypes were grouped as met carriers and compared to those with the val/val. Brain segmentations were obtained from structural magnetic resonance imaging (MRI) using the Freesurfer. Memory performance was assessed with the California Verbal Learning Task (CVLT).
RESULTS
We found a significant diagnosis effect and marginal interaction between diagnosis and BDNF genotype group for both hippocampus volumes and memory performance. BDNF met allele carrier BD patients had smaller hippocampus volumes and reduced performance on multiple CVLT scores compared to MDD patients and HC.
CONCLUSIONS
We provide strong evidence for the BDNF val66met polymorphism as a putative biological signature for the neuroanatomical and cognitive abnormalities commonly observed in BD patients.
Topics: Adult; Alleles; Bipolar Disorder; Brain-Derived Neurotrophic Factor; Depressive Disorder, Major; Female; Genotype; Hippocampus; Humans; Magnetic Resonance Imaging; Male; Memory Disorders; Organ Size; Polymorphism, Single Nucleotide
PubMed: 27018938
DOI: 10.1016/j.jad.2016.03.044 -
Parkinsonism & Related Disorders Mar 2014Detecting very early markers of neurodegeneration that predate the diagnosis of idiopathic Parkinson's disease (PD) is a crucial research topic for the development of... (Review)
Review
OBJECTIVES
Detecting very early markers of neurodegeneration that predate the diagnosis of idiopathic Parkinson's disease (PD) is a crucial research topic for the development of disease-modifying therapeutic interventions. Recently (123)I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy has become widely used for this purpose, since this test shows high sensitivity and specificity in the diagnosis of PD, based on evidence that cardiac sympathetic nerve fibers are affected early and commonly in PD. We reviewed the literature to determine the role of MIBG myocardial scintigraphy for diagnosing pre-motor PD.
METHODS
We performed a systematic review of the literature to identify the use of MIBG myocardial scintigraphy in relation to the constellation of pre-motor symptoms in PD.
RESULTS
Mild memory disorder, autonomic failure (constipation and postural hypotension), depression/anxiety, visual hallucination/psychosis (in the elderly), sleep disorder (REM sleep behavior disorder), and impaired olfaction are reported to appear as sole initial symptoms of PD. All clinical features except for impaired olfaction are accompanied by low MIBG uptake, suggestive of very early PD in situ.
CONCLUSION
Identifying persons with mild memory disorder, constipation/postural hypotension, depression/anxiety, visual hallucination/psychosis (in the elderly), and REM sleep behavior disorder associated with low MIBG uptake may provide a unique opportunity to detect very early PD in situ within a pre-clinical window. Future prospective studies to investigate further the findings of these early cases are warranted.
Topics: 3-Iodobenzylguanidine; Animals; Constipation; Humans; Hypotension, Orthostatic; Memory Disorders; Myocardial Perfusion Imaging; Parkinson Disease; REM Sleep Behavior Disorder; Radiopharmaceuticals
PubMed: 24332912
DOI: 10.1016/j.parkreldis.2013.11.001 -
Journal of the International... Apr 2017Verbal memory (VM) impairment is prominent in bipolar disorder (BD) and is linked to functional outcomes. However, the intricacies of VM impairment have not yet been...
BACKGROUND
Verbal memory (VM) impairment is prominent in bipolar disorder (BD) and is linked to functional outcomes. However, the intricacies of VM impairment have not yet been studied in a large sample of BD patients. Moreover, some have proposed VM deficits that may be mediated by organizational strategies, such as semantic or serial clustering. Thus, the exact nature of VM break-down in BD patients is not well understood, limiting remediation efforts. We investigated the intricacies of VM deficits in BD patients versus healthy controls (HCs) and examined whether verbal learning differences were mediated by use of clustering strategies.
METHODS
The California Verbal Learning Test (CVLT) was administered to 113 affectively stable BD patients and 106 HCs. We compared diagnostic groups on all CVLT indices and investigated whether group differences in verbal learning were mediated by clustering strategies.
RESULTS
Although BD patients showed significantly poorer attention, learning, and memory, these indices were only mildly impaired. However, BD patients evidenced poorer use of effective learning strategies and lower recall consistency, with these indices falling in the moderately impaired range. Moreover, relative reliance on semantic clustering fully mediated the relationship between diagnostic category and verbal learning, while reliance on serial clustering partially mediated this relationship.
CONCLUSIONS
VM deficits in affectively stable bipolar patients were widespread but were generally mildly impaired. However, patients displayed inadequate use of organizational strategies with clear separation from HCs on semantic and serial clustering. Remediation efforts may benefit from education about mnemonic devices or "chunking" techniques to attenuate VM deficits in BD. (JINS, 2017, 23, 358-366).
Topics: Adult; Bipolar Disorder; Female; Humans; Male; Memory Disorders; Middle Aged; Verbal Learning
PubMed: 28382899
DOI: 10.1017/S1355617717000133 -
Journal of Neurodevelopmental Disorders Nov 2023ATRX is an ATP-dependent chromatin remodeling protein with essential roles in safeguarding genome integrity and modulating gene expression. Deficiencies in this protein...
BACKGROUND
ATRX is an ATP-dependent chromatin remodeling protein with essential roles in safeguarding genome integrity and modulating gene expression. Deficiencies in this protein cause ATR-X syndrome, a condition characterized by intellectual disability and an array of developmental abnormalities, including features of autism. Previous studies demonstrated that deleting ATRX in mouse forebrain excitatory neurons postnatally resulted in male-specific memory deficits, but no apparent autistic-like behaviours.
METHODS
We generated mice with an earlier embryonic deletion of ATRX in forebrain excitatory neurons and characterized their behaviour using a series of memory and autistic-related paradigms.
RESULTS
We found that mutant mice displayed a broader spectrum of impairments, including fear memory, decreased anxiety-like behaviour, hyperactivity, as well as self-injurious and repetitive grooming. Sex-specific alterations were also observed, including male-specific aggression, sensory gating impairments, and decreased social memory.
CONCLUSIONS
Collectively, the findings indicate that early developmental abnormalities arising from ATRX deficiency in forebrain excitatory neurons contribute to the presentation of fear memory deficits as well as autistic-like behaviours.
Topics: Female; Mice; Male; Animals; Autistic Disorder; Neurons; Memory Disorders; Cognition
PubMed: 37957569
DOI: 10.1186/s11689-023-09508-7 -
Dialogues in Clinical Neuroscience Dec 2013Memory is an important capacity needed for survival in a changing environment, and its principles are shared across species. These principles have been studied since the... (Review)
Review
Memory is an important capacity needed for survival in a changing environment, and its principles are shared across species. These principles have been studied since the inception of behavioral science, and more recently neuroscience has helped understand brain systems and mechanisms responsible for enabling aspects of memory. Here we outline the history of work on memory and its neural underpinning, and describe the major dimensions of memory processing that have been evaluated by cognitive neuroscience, focusing on episodic memory. We present evidence in healthy populations for sex differences-females outperforming in verbal and face memory, and age effects-slowed memory processes with age. We then describe deficits associated with schizophrenia. Impairment in schizophrenia is more severe in patients with negative symptoms-especially flat affect-who also show deficits in measures of social cognition. This evidence implicates medial temporal and frontal regions in schizophrenia.
Topics: Humans; Memory; Memory Disorders; Schizophrenia; Schizophrenic Psychology
PubMed: 24459407
DOI: 10.31887/DCNS.2013.15.4/rgur -
International Journal of Molecular... Mar 2021Sulforaphane, a potent dietary bioactive agent obtainable from cruciferous vegetables, has been extensively studied for its effects in disease prevention and therapy.... (Review)
Review
Sulforaphane, a potent dietary bioactive agent obtainable from cruciferous vegetables, has been extensively studied for its effects in disease prevention and therapy. Sulforaphane potently induces transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated expression of detoxification, anti-oxidation, and immune system-modulating enzymes, and possibly acts as an anti-carcinogenic agent. Several clinical trials are in progress to study the effect of diverse types of cruciferous vegetables and sulforaphane on prostate cancer, breast cancer, lung cancer, atopic asthmatics, skin aging, dermatitis, obesity, etc. Recently, the protective effects of sulforaphane on brain health were also considerably studied, where the studies have further extended to several neurological diseases, including Alzheimer's disease (AD), Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, autism spectrum disorder, and schizophrenia. Animal and cell studies that employ sulforaphane against memory impairment and AD-related pre-clinical biomarkers on amyloid-β, tau, inflammation, oxidative stress, and neurodegeneration are summarized, and plausible neuroprotective mechanisms of sulforaphane to help prevent AD are discussed. The increase in pre-clinical evidences consistently suggests that sulforaphane has a multi-faceted neuroprotective effect on AD pathophysiology. The anti-AD-like evidence of sulforaphane seen in cells and animals indicates the need to pursue sulforaphane research for relevant biomarkers in AD pre-symptomatic populations.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Biomarkers; Cell Line, Tumor; Disease Models, Animal; Drug Administration Schedule; Drug Evaluation, Preclinical; Gene Expression Regulation; Humans; Isothiocyanates; Memory Disorders; Neurons; Neuroprotective Agents; Oxidative Stress; Protein Aggregates; Sulfoxides; tau Proteins
PubMed: 33805772
DOI: 10.3390/ijms22062929 -
Schizophrenia Bulletin Jan 2016Meta-analyses and reviews on cognitive disorders in schizophrenia have shown that the most robust and common cognitive deficits are found in episodic memory and... (Meta-Analysis)
Meta-Analysis Review
Meta-analyses and reviews on cognitive disorders in schizophrenia have shown that the most robust and common cognitive deficits are found in episodic memory and executive functions. More complex memory domains, such as autobiographical memory (AM), are also impaired in schizophrenia, but such impairments are reported less often despite their negative impact on patients' outcome. In contrast to episodic memory, assessed in laboratory tasks, memories of past personal events are much more complex and directly relate to the self. The meta-analysis included 20 studies, 571 patients with schizophrenia spectrum disorder, and 503 comparison subjects. It found moderate-to-large effect sizes with regard to the 3 parameters commonly used to assess AM: memory specificity (g = -0.97), richness of detail (g = -1.40), and conscious recollection (g = -0.62). These effect sizes were in the same range as those found in other memory domains in schizophrenia; for this reason, we propose that defective memories of personal past events should be regarded as a major cognitive impairment in this illness.
Topics: Executive Function; Humans; Memory Disorders; Memory, Episodic; Mental Recall; Psychiatric Rehabilitation; Schizophrenia; Schizophrenic Psychology; Self Concept
PubMed: 26209548
DOI: 10.1093/schbul/sbv099